Two phases of the overall project described in previous years work were rounded out for publication. The choline+ and CA++ stimulated secretion of 3H-NE in adrenergic nerve endings in rat heart ventricle slices was inhibited by ATP and other triphosphory lated nucleosides. A new aspect of this problem was begun. The effect of ATP was antagonized by N-ethyl-maleimide, chlorpromazine and 2, 4-DNP. The inhibiton of secretion by the transport inhibitors, cocaine and desipramine, was Na+-dependent and antagonized by K+. The antagonism by K+ could explain why neurotransmission is not strongly, if at all, antagonized by transport inhibitors. Evidence suggests that the outward transport of NE during Ch+-Ca++ stimulation is mediated by a different mechanism than that which mediates the uptake of NE.